The invention described in this application pertains to the class of medical devices used to treat heart disease that function to decrease the size of the heart, or to prevent enlargement of the heart.
Heart disease is common in our society, and the incidence is rapidly increasing. One class of heart disease, heart failure, affects 4 to 5 million patients in the United States, with up to two million hospitalizations per year. This accounts for 2 to 3 percent of the national healthcare budget. The American Heart Association reports a continue increase in the incidence of heart failure in the United States, with 51,546 deaths reported in 2000. There were 999,000 hospital discharges with diagnosis of congestive heart failure (ICD/9 428.0, ICD10/150.0) in year 2000, at an estimated healthcare cost of US$24.3 billion. There were 27,213 deaths from cardiomyopathy (ICD/9 425, ICD/10 142), (87% either congestive or dilated) in 2000, with total mentioned mortality of 54,900, and 31,000 hospital discharges.
Causes of cardiomyopathy and congestive heart failure include hypertension, valvular heart disease, and ischemic heart disease, manifest by left ventricular aneurysms or global enlargement of the left ventricle. Other causes of heart failure include some forms of congenital heart disease, viral cardiomyopathy, where the heart enlarges secondary to a viral infection, and idiopathic dilated cardiomyopathy, where the heart enlarges for unknown reasons.
In the early stages of heart disease the body conserves sodium by limiting excretion in the kidney. This increases the volume of blood presented to the heart. As described by the Frank-Starling mechanism, the heart works more efficiently with mild dilatation. However, this mechanism becomes ineffective, and actually deleterious, beyond a mild degree of dilatation. Excessive volume of blood and increased filling pressures may actually cause progressive dilatation of the heart. A vicious cycle of increased blood volume resulting in increased heart failure resulting in increased blood volume, etc., is started. The heart is particularly susceptible to dilatation from excessive pressure and volume during diastole, the period of the cardiac cycle when the heart is at rest.
The medical treatment of heart disease includes restriction of the oral intake of sodium, diuretic medications, direct vasodilators, and inhibitors of angiotensin converting enzyme. These modes of therapy are directed at decreasing the volume of blood in the circulatory system and the dimensions of the heart. As derived from physiological Law of LaPlace, the larger the heart is, the greater wall tension is required to generate a certain pressure within the heart. Remodeling, a term used to describe abnormal enlargement of the heart, causes the heart to function less efficiently. Greater energy or work is needed to generate satisfactory blood pressure and blood flow.
Although the medical treatment for heart disease and heart failure has progressed over the last decade, many patients require surgical therapy. Conventional surgical therapy includes coronary artery revascularization, valve repair or replacement, and treatment of ventricular aneurysms. Although many patients benefit significantly from surgery, some patients have progressive or continued cardiac enlargement. None of the modes of conventional cardiac surgery directly prevent progressive or persistent dilatation of the heart.
A recent report Bolling and others describes a high-risk group of patients with severely dilated hearts who undergo repair or replacement of the regurgitant mitral valve. This report demonstrates the feasibility of performing successful operations on such very sick patients. This report also demonstrates that the heart may shrink in size when excessive volume of blood in the heart is treated. Unfortunately, not all of the patients in this group had significant of long-term benefit, and some required transplantation. The use of the device(s) described in this patent application should prevent persistent and/or recurrent dilatation of the left ventricle in patients such as these.
An uncommon yet fatal complication of myocardial infarction is rupture of the left ventricle. The left ventricle can rupture in the free wall causing a cardiac tamponade, or it may rupture into the right ventricle, causing an ischemic ventricular septal defect. Currently there is no medical device that can be used to treat this fatal disease. The device described in this patent application could be used to treat this condition and effectively seal the rupture of the left ventricle.
An operation to remove a portion of the left ventricular wall was popularized in the mid 1990s by Randas Batista. This operation made the left ventricular chamber smaller, which allowed for improved hemodynamic function. Many patients underwent this surgical procedure, but most had recurrent dilated heart disease. The use of the invention described in this application in such a group of patients either as an alternative to this operation or in conjunction with this operation might prove beneficial.
A group of patents (U.S. Pat. Nos. 6,439,237; 6,221,104; 6,024,096) were recently issued pertaining to a specialized technique of repair of ventricular aneurysms. After removal of excessive scar tissue from the aneurysm, a specialized patch is used to repair the aneurysm. This technique surgically decreases the size of the left ventricle, but unfortunately does not prevent progressive and recurrent dilatation of the heart. The device(s) described in this patent application might be used to augment the conventional repair of a ventricular aneurysm, preventing progressive or recurrent dilatation of the heart.
The concept of wrapping the heart with skeletal muscle, or dynamic cardiomyoplasty, was popularized in the last two decades. Only minimal improvement of the cardiac output is seen with this operation in both animals and humans. The benefit, if any, of this procedure likely comes from constraining or squeezing the heart to a smaller size. This operation does not directly limit the filling of the heart with blood. The device(s) described in this patent application might be used instead of dynamic cardiomyoplasty to treat these patients with heart disease.
One satisfactory means of treatment of extreme cases of heart disease is heart transplantation. There are unfortunately a limited number of donors, and only a very small fraction of patients who would benefit from heart transplantation are able to receive a donor heart. Heart transplantation requires immunosuppression, which has many serious and sometimes fatal side effects. Heart transplantation is extremely expensive, with the initial cost of approximately US$150,000 to 200,000, and recurrent yearly costs of approximately US$25,000 to 40,000. The average lifespan of a patient after heart transplant is 8 years.
An ever-expanding mode of therapy for advance heart disease is the use of a mechanical pumping device. These pumps were first used in the 1960s, and literally dozens of different types of pumps are currently in use or in various stages of development. These pumps are used either to assist the diseased heart or to completely replace the heart. Currently, the use of mechanical cardiac assist devices is limited by frequent and common complications of the implantation and use of the devices. The complications include thrombosis, thrombotic emboli causing stroke, organ, and limb ischemia, infection, particularly from the driveline, as well as catastrophic mechanical failure of the device. Furthermore, these devices are extremely expensive, with some costing approximately US$85,000.
Jarvik has described a novel use of mechanical pumping devices (U.S. Pat. No. 5,092,879) by placing the pump within the confines of the left ventricle. One embodiment of his invention is a muscle powered blood pump placed within the left ventricle of the heart. This device utilizes skeletal muscle excited by a pacemaker, wrapped around a complex sac. Unlike Jarvik's invention, the blood sac of the present invention very simple in design and construction. The sac is activated by the native heart, and does not require autotransplantation or homotransplantations of muscle tissue into the heart. The current invention allows for improvement of a diseased heart by limiting filling of the heart during diastole.
An intraventricular rotary blood pump is now in clinical use (Jarvik, U.S. Pat. No. 5,824,070), but with only modest improvement of the patients, and an important rate of complications. These intraventricular blood pumps do not directly or precisely limit filling of the left ventricular chamber of the heart.
A new class of medical devices has been developed to physically alter the shape and size of the heart. One group of such devices (U.S. Pat. Nos. 5,957,977; 6,190,408; 6,221,103; 6,409,760; 6,520,904) fit around and within the interior of the left ventricle to constrain the heart to a more normal size and shape. The multiple internal and external rigid members of this complex device press directly on the tissue of the heart. These devices may erode into the vital structure of the heart, possibly even perforating the heart. This device does not directly limit the volume of blood entering the left ventricle. Only modest improvement of cardiac function has been shown in a recent animal study reported by Kashem and others.
Another similar group of devices are placed on the surface to the heart (U.S. Pat. Nos. 6,332,864; 6,264,602; 6,183,411; 6,402,680; and 6,402,67X). These devices attempt to reshape and reduce the size of the heart. The rigid parts of these devices have the potential to erode into the vital structure of the heart, possibly even perforating the heart. These devices do not directly limit the volume of blood entering the left ventricle.
Yet another group of devices (U.S. Pat. Nos. 6,537,198; 6,514,194; 6,406,420; 6,332,893; 6,332,863; 6,261,222; 6,260,552; 6,165,120; 6,165,119; 6,162,168; 6,077,214; 6,059,715; 6,050,936; 6,045,0497; and 5,961,440) attempt to reshape the heart with a wire or wires traversing the left ventricular chamber of the heart. These devices have the potential to disrupt the mitral valve and subvalvular apparatus, as well as the potential to erode into other vital structure of the heart, possibly even perforating the heart. There is a potential for bleeding from the wires puncturing the left ventricular chamber of the heart. These devices do not directly limit the volume of blood entering the left ventricle of the heart. These devices do not prevent further dilatation of the heart, nor do they direct shrinking or reverse remodeling of the heart. Only modest improvement of cardiac function has been demonstrated in recent studies, as reported by Schenk and others.
Another series of devices described by Clifton Alferness (U.S. Pat. Nos. 6,537,203; 6,482,146; 6,375,608; 6,370,429; 6,241,654; 6,230,714; 6,169,922; 6,165,122; 6,165,121; 6,126,590; 6,123,662; 6,085,754; 6,077,218; and 5,702,343), Kay Nauertz and others (U.S. Pat. No. 6,155,972), Michael Girard (U.S. Pat. No. 6,174,279), Kurt Krueger (U.S. Pat. No. 6,193,648), Edward Shapland and others (U.S. Pat. No. 6,425,856), and Hans Handle (U.S. Pat. No. 6,416,459) consist of a bag which wraps around the heart to constrain the heart to a more favorable size and shape. The device has the potential to slip out of position, to constrict the heart, and to cause formation of scar tissue around the heart. This series of devices does not directly or precisely limit filling of the left heart with blood. Early reports on this series of devices have shown only marginal benefit.
It has been reported by Burkoff and other groups that the left ventricle of the heart will return to normal size when circulation is supported with a left ventricular assist device. A left ventricular assist device is a mechanical pump that augments the pumping action of the heart. Many patients who have had previous placement of a ventricular assist device benefit by shrinking of their enlarged heart to a more normal size and shape. This process of decreasing the size of an abnormally enlarged heart is referred to as “reverse remodeling”. This effect of reverse remodeling demonstrates that if the left ventricle is no longer exposed to excessive pressure and volume of blood, it naturally shrinks to a more normal size and shape.
Some patients who have had significant reverse remodeling after placement of a left ventricular assist device chose to have the device removed. Of these patients who had removal of a device, some have had sustained benefit of the reverse remodeling, although many unfortunately have recurrent progression of their dilated heart disease. The invention described in this application could be used in such a group of patients to treat the heart disease, either used instead of a left ventricular assist device, or placed at the time of removal of the left ventricular assist device to prevent recurrent cardiac enlargement.
Primary pulmonary hypertension is a devastating disease of the heart and the lungs, manifest primarily by right heart failure. The only effective treatment of endstage primary pulmonary hypertension is transplantation of one or both lungs, or combined heart and lung transplantation. The current invention could be used as a treatment for the right heart failure and dilation of primary pulmonary hypertension.
Among the therapies for treatment of an enlarged heart, all strive to make the heart smaller. The purpose of the present invention is to make the ventricle small and/or to keep the ventricle small. The invention partitions the blood within the ventricle to protect the ventricle from the excessive volume and increased pressure of the blood.